In the battle between a cell and a virus, either side may resort to
subterfuge. Molecular messages, which control the cellular machinery
both sides need, are vulnerable to interception or forgery. New research
at Rockefeller University has revealed the unique twist on just such a
strategy deployed by the liver-infecting Hepatitis C virus - one that
may help explain the progression of liver disease and that the
researchers suspect may be found more widely in the world of
disease-causing viruses.

Led jointly by Charles Rice, the Maurice R. and
Corinne P. Greenberg Professor in Virology and head of the Laboratory of
Virology and Infectious Disease and Robert Darnell, Senior Attending
Physician, Robert and Harriet Heilbrunn Professor, and head of the
Laboratory of Molecular Neuro-oncology, the research is described today
(March 12) in Cell. It employed a powerful combination of techniques to map the interactions between the virus and a small piece of genetic material - known as miRNA-122 - that is produced almost exclusively by liver cells, which normally use it to regulate expression of their own genes.

"It is well known that once inside a liver cell, the hepatitis C
virus must bind to miRNA-122 in order to establish a persistent
infection. We found an unanticipated consequence of this interaction: By
binding to miRNA-122, the virus acts like a sponge, soaking up these
gene-regulating molecules," says first author Joseph Luna, a graduate
student with a joint appointment in the labs. "Our experiments showed
this has the effect of skewing gene activity in infected liver cells."